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88 Cards in this Set
- Front
- Back
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Normal flora of the skin
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Staph epi, Anaerobic GPC, Corynebact, Propionibact, Malassezia furfur
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Where do you find gram neg rods on the skin?
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groin, armpits, toes. . . you know . . .
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2 persistant transient skin flora who can do some damage
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Staph aureus
Strep pyogenes |
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How does the skin get infected?
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*There must be a way for the surface colonizers to get in. 3 ways are moisture, trauma, and loss of blood supply
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From outside in--spreading infections
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Impetigo, Erysipelas, Cellulitis
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Spreading abcesses. Who is the likely culprit?
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Folliculitis, Furuncles, Carbuncles
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Infections that result in tissue death
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Necrotizing fasciitis/cellulitis . . . then gangrene . . . and if you're really unlucky myonecrosis
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You become bacteremic, and the colonizers are working their way out . . . what happens? Who is at fault?
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Abscess, necrosis, Exanthem. N. meningitidis, P. aeruginosa, lots and lots of virals that ultimately cause rash (measles, anyone)?
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Catalase positive
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The staph family
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Catalase negative
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The strep family
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Are staph mobile?
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No, thank god
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Coagulase positive
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Staph aureus
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Coagulase negative
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Another undifferentiated staph species, but not aureus
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What role does coagulase actually have?
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It will covert fibrinogen to fibrin (think clotting cascade), thus allowing the infectious organism to wall itself off and form abscesses
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Where on the body will you find staph aureus?
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External nares, skin, vag, feces.
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What tissues can Staph A MSCRAMMS bind to?
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Fibronectin, fibrinogen, elastin, collagen -- it really like the ECM
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How do you indentify staph aur in a laboratory that apparently totally lacks culture agar?
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It will bind to three epitopes on fibrinogen
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Strep pyo and Staph aur can both do what to your epithelium?
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Stimulate uptake by nonphagocytic cells. It's a survival technique
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What can you do to minimize risk of staph aur in daily life?
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WASH YOUR HANDS.
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The peptidoglycan layer of staph aur is recognized by what?
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TLR-2, which probably kills infections with the innate immune system most of the time.
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Virulence genes in staph aureus are guided by what?
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The AGR locus. Screw with the locus, and staph aureus becomes much weaker.
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Protein A structural component of staph aur?
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Binds the Fc portion of antibodies.
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Hyaluronidase/Staphylokinase/lipase roles in staph aureus?
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Liquify the ECM so the infection can spread
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Scalded skin syndrome
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The exfoliative toxin of staph aureus. It's not inflammatory, just irritating. You should drink a lot to minimize water loss.
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TSST
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Superantigen toxin of staph aureus. Luckily, most of us possess antibodies to it.
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Staph aureus enterotoxin
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Superantigen. Food poisoning if you eat it.
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Panton-Valentine Leukocydin
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Just what it sounds like. It will eat a hole in the membrane of PMNs and others. Major toxicity.
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If you do not have neutrophils. . .
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You are a walking staph aureus target.
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Clinical picture of TSS
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Like any inside out bacteremic infection -- diarrhea, vomiting, headache, hypotension from water loss, erythematous rash, desquamation. It can be ftal.
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Important clinical sequelae of staph aureus
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Endocarditis - IV drug users
Septic arthritis Necrotizing aspirated pneumonia |
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Will you know if you're eating food contaminated with staph aureus?
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Not a clue. So watch the innocent potato salad.
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How do the coagulase neg staphs cause infections?
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They use entry portals, like catheters and prostheses and artificial valves. They mostly slime up to protect themselves, and you will have to remove the infected device.
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Treating a staph infection
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1. Drain the abscess
2. Since they're all beta-lactamase producers, you could use methicillin 3. But then there's MRSA due to mecA gene. 4. Vanco, linezolid, dapto, trimeth/sulf |
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Community Acquired MRSA has a nasty new mutation that . . .
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. . . will actually "call" neutrophils to kill them.
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Gram neg anaerobes
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Bacteroides fragilis, fusobacterium, prevotella
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Gram poz anaerobes
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Peptostrep, Clostridium
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How do the gut flora typically cause infections?
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They are released into a multimicrobial environment by trauma or damage, and the aerobes helpfully consume all the local oxygen, making the new area perfect for anaerobic colonization.
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Where will you rarely recover anaerobes as pathogens?
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Urine, CNS, acute respiratory infection
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Does anaerobic infection smell bad?
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Yes.
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How can you get an anaerobic infection say, in a bar fight?
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Someone bites you. Their gut/oral flora get into the wound.
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DOC for bacteroides?
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Metronidazole
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You have an infection/wound/trauma where you suspect anaerobic infiltration (bad smell, necrosis imminent) from the gut. What is the number one offender?
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Bacteroides fragilis
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Typical treatment for ALL gut anaerobic infections outside the gut?
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Surgical. They are mad hard to get rid of otherwise.
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Physical appearance of the clostridium perfringens in gram stain?
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Boxcars. They do sporulate, but not in active infections.
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How can you remember clostridium perfringens is a gut anaerobe?
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PERFORATED by perfringens = gangrene
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Key toxin of clostridium perfringens
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alpha toxin: lecithinase, eats cell membranes of everyone.
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Who is at risk for clostridium gangrene?
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Recent surgical patients, diabetics
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What is crepitant cellulitis/gas gangrene?
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Unlike staph aur, clostridium causes gangrene and produces gas via anaerobic metabolism. The gas sounds crackly. Staph aureus, being an aerobe, will cause gangrene that doesn't make noise.
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How fast is gas gangrene?
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Hours. Very rapid. Toxin eats everything in its path. Fortunately this is rare, but unfortunately it requires disfiguring surgical debridement/amputation to clear.
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Plate diagnosis of clostridium perf
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Double zone hemolysis, alpha and theta toxins both cause individual cell death.
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What is helpful as a supportive treatment for clostridium?
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Oxygen.
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Appearance of clostridium tetani under a scope?
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Little tennis rackets
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Lethal toxin of clostridium tetani?
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Tetanospasmin.
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Diagnosing tetanus?
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If you suspect it, treat it. You can very rarely isolate a strict anaerobe.
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2 clos tetani intros into body
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Puncture wound or umbilical contamination
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Pathogenesis of tetanospasmin toxin
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Binds to CNS, irreversible. Retrograde carried into brain, then diffuses and blocks all inhibitory neurotransmitter release.
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First sign of tetanus
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Masseteric rigidity. Lockjaw
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Will tetanus knock you out?
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Unfortunately, no.
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How can you die from tetanus?
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Respiratory paralysis and failure, or you die from malnutrition
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How do neonates get tetanus?
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From their unvaccinated moms. This is a fatal and devastasting disease that's easily preventable.
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Treatment of an active tetanus infection?
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Nutrition, antibodies to toxin, benzos, antibiotics, then immunize them.
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is there a lasting immunity to tetanus?
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No. A mounted immune response to the toxin during the active disease is abortive and incomplete.
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Chronic swimming pool or water-source infection?
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Mycobacterium marinum. Ulcerating papules that can take months to clear. You will see acid-fast bacilli.
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Nosocomial bacteria that causes draining skin lesions, chronic but rapid.
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Mycobacterium fortuitum/chelonae, abscessus. Think FORTUITous advantage of your hospital weakened state.
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What's lucky about all the mycobacterium infections?
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They like it cold, so their growth at physiological temp (and therefore invasive potential) is very slow
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Characteristics of mycobacterium leprae?
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Obligate intracellular, grows very slowly, tropism for nerves, never cultured in vitro, need a lot of long, close contact to acquire.
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Tuberculoid leprosy
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Synonymous with paucibacillary leprosy. Better prognosis
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Leprematous leprosy
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Synonymous with multibacillary leprosy. Poor prognosis
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Can a TH2 response help with leprematous leprosy?
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No, you need a TH1 response but the bacteria is adept at pushing it the other way.
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Can you activate a leprosy-filled macrophage?
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No. It cannot be activated to kill the intracellular invader.
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Clinical appearance of multibacillary leprosy?
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Skin patches, thickening, edematous nerve involvement.
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Clinical appearance of paucibacillary leprosy?
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Plaques without feeling, granulomas (due to successful TH1 response), will be immuno-sufficient.
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Long-term sequelae of leprosy
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Peripheral and facial deformity due to nerve deficits
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Antileprematous drugs
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Dapsone, rifampicin, clofazimine. You want to treat with more than one drug, and sometimes all 3 with serious multibacillary.
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Problem with treating leprosy
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As the immune system "wakes up", you will have additional inflammatory complications. It may be necessary to immunosuppress with steroids.
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Superficial noninflammatory fungal infection of note
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Pityriasis (sometimes called tinea) versicolor. Caused by Malassezia Furur. It's a yeast, it causes macular lesions of multicolors, use miconazole
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3 common dermatophytes
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1. Microsporum - hair/skin
2. Trichophyton - hair/skin/nails 3. Epidermophyton Floccosum - skin/nails |
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Clinical appearance of dermatophytes
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Scaly lesions that, since they don't provoke any immune response, can be a bitch to cure. Tinea is the common prefix for these diseases. Go to the topical azoles once you see hyphae. Lamisil, anyone?
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Trauma-induced subcutanous skin infections?
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Sporothrix schenkii - pricked by a rose. cigar-yeast. Painless small lesions that follow the lymph and last for years. Use Itraconazole.
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Viral cutaneous disease with 2 week incubation and prevesicular contagion?
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VZV.
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When you get over chickenpox. . .
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VZV runs to the DRG and goes to sleep until much later in life, you can develop shingles.
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Chickenpox while pregnant?
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Is a bad thing. VZV takes advantage of the immunocompromised like any Herpesviridaie, and the fetus has no immune response to speak of. Large range of congenital birth defects.
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Clinical presentation of Zoster?
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Dermatome pain some days in advance, followed by lesions along the dermatome. Excruciating. Slow to heal.
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Dangerous sequelae of Zoster?
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Keratitis via cranial nerve involvement. Blindness.
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Treatment of Zoster?
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Acyclovir, Famcyclovir, Valacyclovir
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Should you recommend the Zostavax vaccine even to patients who have had chickenpox?
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Yes, later in life. It may prevent Zoster outbreaks.
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Is there any risk for an older patient who has had chickenpox hanging out with a chickenpox infected kid?
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No. VZV reactivation has nothing to do with disease exposure.
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Trichinosis
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Cyst protozoa you can get from uncooked pork. Cysts deposit and cause a wide variety of symptoms. It sucks.
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